Methanococcoides sp. SA1
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA632496 | ENA |
REPOSITORIES: ENA
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Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS. Examination of genome wide distribution of cohesin subunits in wildtype and SA1-null cells
2012-03-15 | E-GEOD-32319 | biostudies-arrayexpress
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS.
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Project description:Eggplant is susceptible to fungal wilts caused by Fusarium oxysporum f. sp. melongenae and Verticillium dahliae. Wild relatives represent a good source of resistance and ILs have been obtained through introgression of the Rfo-sa1 locus conferring resistance to Fusarium oxysporum from the allied species S. aethiopicum into cultivated eggplant. In this work, a deep phenotypical characterization was performed according to the progression of symptoms along the stem and the disease severity in leaves. This analysis showed that the Fom -resistant ILs carrying introgression of the Rfo-sa1 locus displayed significantly improved tolerance to Verticillium attack after a preliminary inoculation with F. oxysporum. This positive effect was particularly evident when Verticillium inoculation was done simultaneously or after the Fusarium one. Transcript profiling carried out using a combination of SSH, microarray and qRT-PCR analyses from inoculated roots with a selected combinations of fungal pathogens enabled the identification of 164? differentially expressed genes at least in one condition. Overall, our results highlighted a number of candidate genes putatively involved in early defence responses or signalling pathways activated upon infection of eggplant either with Fom and Vd and thus leading to a broad Rfo-sa1 mediated tolerance against both these wilt pathogens.
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